Arterial Chemoreflex influence in Cardiac Energetics

The arterial chemoreflex is a negative feedback mechanism that regulates the ventilatory responses to changes in arterial oxygen and carbon dioxide concentrations, sensed by carotid chemoreceptors. Whenever the arterial pressure of oxygen increases above a critical level, parasympathetic nervous activity increases, contributing a decrease in heart rate and arterial blood pressure. As the chemoreflex influences cardiac output to compensate for changes in oxygen arterial pressure, we hypothesized that it must influence the mechanical interaction between the left ventricle and the arterial tree, as well as cardiac energy consumption and efficiency. The ventriculo‐arterial coupling was evaluated on a beat‐per‐beat basis, upon the application of lobeline in the left‐carotid sinus of anesthetized, paralyzed and artificially ventilated rabbits. An intraventricular impedance catheter was used to measure simultaneously ventricular pressure and volume. All experiments were performed according to national laws and international guidelines. We designed a custom software to characterize single‐beat left‐ventricular and arterial physiologic properties. From this data, left‐ventricle end‐systolic elastance (Ees), arterial elastance (Ea) and the coupling ratio (Ea/Ees) were computed to analyze ventriculo‐arterial coupling. We also calculated left‐ventricular stroke work (SW), total energy expenditure (PVA), ratio of the SW to its theoretical maximum (Qload) and cardiac work efficiency (CWE=SW/PVA). Upon the application of the carotid chemoreflex, Ees and Ea both increased, though without any noticeable change in their coupling ratio (Ees/Ea). Stroke work and total energy consumption (oxygen demand) both decreased, without sacrifice of the mechanical and energetic efficiency of the heart. Ventriculo‐arterial coupling was maintained in the interval of optimal cardiac efficiency. For statistical analysis with paired Student's t‐test, please refer to Table 1. In conclusion, the arterial chemoreflex is a control mechanism of the cardiovascular system that exerts a feedback modulation on ventilatory responses through an increase in both cardiac contractility and arterial input impedance, in such a balance that ventriculo‐arterial coupling, mechanical and energetic efficiency are maintained between optimal values. This approach can now be applied to test acute interventions on the circulatory system, including diseases such as myocardial infarction, drug and device therapy. Support or Funding Information PHYSIOMAT ‐ Modelação Matemática e Computacional da Fisiologia Humana (2013) Fundação para a Ciência e Tecnologia EXCL/MAT‐NAN/0114/2012 1 Mean and standard deviation of cardiac parameters before and after lobeline injection, and p‐values from paired Student's t‐test.baseline (20 beats) after injection (20 beats) p‐value (paired t‐test)Arterial pressure mmHg 92 ± 3.258 102 ± 6.283 <0.001Instantaneous Heart Rate bpm 243 ± 0.923 235 ± 4.528 <0.001Arterial elastance (Ea) mmHg/mL 71.143 ± 3.085 79.450 ± 6.195 <0.001End‐systolic elastance (Ees) mmHg/mL 59.736 ± 1.990 71.001 ± 6.423 <0.001Ventriculo‐arterial coupling (Ea/Ees) ‐ 1.188 ± 0.062 1.142 ± 0.097 0.23Ejection fraction (EF) % 45 ± 1.289 47 ± 1.262 0.22Stroke volume (SV) mL 1.456 ± 0.034 1.221 ± 0.135 <0.001Stroke work (SW) mmHg * mL 148.621 ± 4.717 136.506 ± 10.595 <0.001Total energy expenditure (PVA) mmHg * mL 234.629 ± 9.483 219.733 ± 16.439 0.001Stroke work to its maximum (Qload) ‐ 0.992 ± 0.005 0.994 ± 0.004 0.20Cardiac work efficiency (CWE) % 63 ± 0.012 62 ± 0.033 0.15